RELATION OF THE PORTAL BLOOD TO LIVER MAINTENANCE
RELATION OF THE PORTAL BLOOD TO LIVER MAINTENANCE
复制标题
门静脉血与肝脏维护的关系
DOI：
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发表时间：
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影响因子：
15.3
通讯作者：
Louise D. Larimore
中科院分区：
文献类型：
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作者：
P. Rous;Louise D. Larimore
兔部分肝脏的门静脉分支闭塞导致门静脉血缺乏区域的实质进行性并最终完全萎缩，并导致接受过量血液的其余肝组织肥大。因此，四分之三的肝脏可以在2个月内减少到纤维标签，而剩余的四分之一则获得整个原始器官的大部分。萎缩是简单的，不伴有明显的退行性改变或任何结缔组织替代。更重要的是，它本质上是有条件的，当增殖组织的胆管被结扎并以这种方式检查其肥大时，它不会进展。文献中有迹象表明，在局部门静脉阻塞后，会发生以肥大为条件的萎缩，如本文所述。在我们实验室里进行的一些尚未完成的实验，明确地表明了它在狗身上的发生。这种变化在犬的肝脏中缓慢发生。3个月后，没有门静脉血的组织减少到原来体积的三分之一。这种萎缩的条件性特征可以通过以下事实来证明：在缺乏代偿性实质的情况下，它不会发生任何类似程度的萎缩，就像门静脉血流通过Eck瘘从整个肝脏转向时一样。萎缩是功能性的吗？如果是这样的话，它的完整性将表明肝脏没有必要的活动--没有维持肝脏的活动所依赖的活动--它与来自门脉系统排出的器官的物质没有密切的联系。观察门静脉流局部改道后的肥大率和萎缩组织分泌的胆汁的性质，可以支持这种观点。肥大的速度几乎，甚至可能相当快，就像从身体中取出没有门静脉血的组织一样。当肝组织萎缩到一定程度，并与大量接受整个门脉血流的肝实质竞争时，其分泌的胆汁几乎是无色的，可能只产生微弱的佩腾克反应。另一方面，糖原在萎缩细胞中的含量和分布与同一动物的肥大肝组织中的含量和分布大致相同。肝实质移位是伴随着门脉血流的局部紊乱而发生的，这一事实与正常肝脏形状的某些改变有关，迄今为止，这些改变一直被粗略地归因于周围器官的压力。它也与病理变化有关。病理学家早就知道肝脏肥大依赖于先前的破坏。现在还必须考虑到一种依赖于代偿性肥大的破坏。后一种性质的变化的发生可以解释某些疾病中观察到的病变，这些疾病涉及到肝实质部分的门脉血流紊乱。
The occlusion of portal branches to a part of the liver of the rabbit leads to a progressive and ultimately complete atrophy of the parenchyma in the region deprived of portal blood, and to hypertrophy of the rest of the hepatic tissue which receives such blood in excess. Three-fourths of the liver may thus be reduced to a fibrous tag within 2 months, while the remaining fourth attains the bulk of the entire original organ. The atrophy is simple, unaccompanied by obvious degenerative changes or by any connective tissue replacement. More important, it is conditional in nature, failing to progress when the bile duct from the proliferating tissue is ligated and its hypertrophy checked in this way. There are indications in the literature that an atrophy conditional on hypertrophy, such as is here described, occurs in man after local portal occlusion. And some experiments in our laboratory, not yet completed, show definitely its occurrence in the dog. The changes take place slowly in the canine liver. After 3 months the tissue deprived of portal blood has diminished to about one-third of its original bulk. The conditional character of the atrophy is proven by its failure to occur to any similar degree in the absence of a compensating parenchyma, as when the portal stream is diverted from the whole liver by way of an Eck fistula. Is the atrophy functional? If so, its completeness would indicate that the liver has no essential activity—none on which its maintenance depends—that it is not intimately connected with substances derived from organs drained by the portal system. Observations on the rate of hypertrophy after local diversion of the portal stream and on the character of the bile secreted by the atrophic tissue may be taken to favor such a view. The hypertrophy is nearly, perhaps quite, as rapid as if the tissue deprived of portal blood had been removed from the body. The bile secreted from a liver mass far advanced in atrophy and competing with a large bulk of parenchyma that receives the entire portal stream is almost colorless and may give but a weak Pettenkofer reaction. Glycogen, on the other hand, is present in the atrophic cells in approximately the same amount and distribution as in the hypertrophic liver tissue of the same animal. The fact that a parenchymal shift follows local disturbances in the portal stream has a bearing on the cause of certain alterations in the shape of the normal liver that have been loosely attributed heretofore to pressure from the surrounding organs. It also has some interest in connection with pathological changes. Liver hypertrophy dependent on a preceding destruction has long been known to pathologists. Now a type of destruction dependent on compensatory hypertrophy must also be reckoned with. The occurrence of changes of the latter character will explain certain of the lesions observed in diseases that involve a disturbance of the portal flow to portions of the liver substance.